Gene-environment interactions in celiac disease: the role of the intestinal epithelium
The intestinal epithelium functions as an active interface integrating genetic susceptibility and environmental signals in celiac disease, beyond its role as an immune injury target.
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What the study showed
The review synthesizes evidence that gluten and HLA genotype are necessary but not sufficient for celiac disease development. Environmental factors such as gut microbiota, infections, and early-life ecosystem modulate disease risk and severity. Intestinal epithelial cells (IECs) release tissue transglutaminase 2 (TG2), participate in antigen presentation, and respond to microbial and dietary cues.
How it was done
Narrative review synthesizing emerging data on gene-environment interactions in celiac disease, with emphasis on the active role of the intestinal epithelium.
Risk of bias
This is a narrative review subject to literature selection bias; the abstract does not report inclusion criteria or a systematic search strategy. Knowledge gaps and areas of active debate are acknowledged by the authors themselves.
What this study does NOT prove
The review does not demonstrate that modulation of the microbiota or environmental factors prevents or treats celiac disease.
In clinical practice
No direct clinical recommendations follow from this review; the roles of IECs and gut microbiota in celiac disease remain under investigation. Interventions targeting these mechanisms lack established clinical support.
Limitations
This is a narrative review subject to literature selection bias; the abstract does not report inclusion criteria or a systematic search strategy. Knowledge gaps and areas of active debate are acknowledged by the authors themselves.
Technical appendix
Version history
- 1.0 · 2026-08-17 — Auto-generated under Evidence Standard v1.0
Paid access: structured summary from public metadata; consult the original study at the source.